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10.2337/db15-0453 http://scihub22266oqcxt.onion/10.2337/db15-0453 C5314719!5314719!26647385     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Diabetes 2016 ; 65 (3): 633-46 Nephropedia Template TP {{tp|p=26647385|t=2016. Restoration of Nrf2 Signaling Normalizes the Regenerative Niche |pdf=|usr=}}{{26647385}} gab.com Text Restoration of Nrf2 Signaling Normalizes the Regenerative Niche JO: Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=26647385 #FOAvip Chronic hyperglycemia impairs intracellular redox homeostasis and contributes to impaired diabetic tissue regeneration. The Keap1/Nrf2 pathway is a critical regulator of the endogenous antioxidant response system, and its dysfunction has been implicated in numerous pathologies. Here we characterize the effect of chronic hyperglycemia on Nrf2 signaling within a diabetic cutaneous regeneration model. We characterized the effects of chronic hyperglycemia on the Keap1/Nrf2 pathway within models of diabetic cutaneous wound regeneration. We assessed reactive oxygen species (ROS) production and antioxidant gene expression following alterations in the Nrf2 suppressor Keap1 and the subsequent changes in Nrf2 signaling. We also developed a topical small interfering RNA (siRNA)?based therapy to restore redox homeostasis within diabetic wounds. Western blotting demonstrated that chronic hyperglycemia?associated oxidative stress inhibits nuclear translocation of Nrf2 and impairs activation of antioxidant genes, thus contributing to ROS accumulation. Keap1 inhibition increased Nrf2 nuclear translocation, increased antioxidant gene expression, and reduced ROS production to normoglycemic levels, both in vitro and in vivo. Topical siKeap1 therapy resulted in improved regenerative capacity of diabetic wounds and accelerated closure. We report that chronic hyperglycemia weakens the endogenous antioxidant response, and the consequences of this defect are manifested by intracellular redox dysregulation, which can be restored by Keap1 inhibition. Targeted siRNA-based therapy represents a novel, efficacious strategy to reestablish redox homeostasis and accelerate diabetic cutaneous tissue regeneration. Twit Text FOAVip Restoration of Nrf2 Signaling Normalizes the Regenerative Niche ????Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=26647385 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26647385 #FOAvip English Wikipedia <ref>{{Cite pmid|26647385}}</ref> Restoration of Nrf2 Signaling Normalizes the Regenerative Niche #MMPMID26647385 Soares MA; Cohen OD; Low YC; Sartor RA; Ellison T; Anil U; Anzai L; Chang JB; Saadeh PB; Rabbani PS; Ceradini DJ Diabetes 2016[Mar]; 65 (3): 633-46 PMID26647385show ga Chronic hyperglycemia impairs intracellular redox homeostasis and contributes to impaired diabetic tissue regeneration. The Keap1/Nrf2 pathway is a critical regulator of the endogenous antioxidant response system, and its dysfunction has been implicated in numerous pathologies. Here we characterize the effect of chronic hyperglycemia on Nrf2 signaling within a diabetic cutaneous regeneration model. We characterized the effects of chronic hyperglycemia on the Keap1/Nrf2 pathway within models of diabetic cutaneous wound regeneration. We assessed reactive oxygen species (ROS) production and antioxidant gene expression following alterations in the Nrf2 suppressor Keap1 and the subsequent changes in Nrf2 signaling. We also developed a topical small interfering RNA (siRNA)?based therapy to restore redox homeostasis within diabetic wounds. Western blotting demonstrated that chronic hyperglycemia?associated oxidative stress inhibits nuclear translocation of Nrf2 and impairs activation of antioxidant genes, thus contributing to ROS accumulation. Keap1 inhibition increased Nrf2 nuclear translocation, increased antioxidant gene expression, and reduced ROS production to normoglycemic levels, both in vitro and in vivo. Topical siKeap1 therapy resulted in improved regenerative capacity of diabetic wounds and accelerated closure. We report that chronic hyperglycemia weakens the endogenous antioxidant response, and the consequences of this defect are manifested by intracellular redox dysregulation, which can be restored by Keap1 inhibition. Targeted siRNA-based therapy represents a novel, efficacious strategy to reestablish redox homeostasis and accelerate diabetic cutaneous tissue regeneration. äRestoration of Nrf2 Signaling Normalizes the Regenerative Niche (epmc).pdf DeepDyve Pubget Overpricing